In vitro evaluation of the potential toxic effects of palladium nanoparticles on fibroblasts and lung epithelial cells

- Palladium nanoparticles inhibited cell growth of Rat-1 and A549 cell lines in a dose- and time-dependent manner;
- Palladium nanoparticles caused a progressive arrest of both cell lines in G0/G1 phase of cell cycle without apoptosis;
- Palladium nanoparticles were able to induce an increase in DNA single strand breaks in Rat-1 and A549 cell lines;
- Exposure to palladium nanoparticles caused a slight increase in the intracellular ROS levels in both cell lines;
- Palladium nanoparticles modulated important cell cycle regulatory proteins in Rat-1 and A549 cell lines.

Palladium nanoparticles have been increasingly used in catalytic processes, wastewater treatment, electronics, and biomedicine. However, recent evidence proved that these nanoparticles are able to induce adverse effects both in in vitro and in vivo models. Nevertheless, molecular mechanisms underlying the toxic effects are still poorly understood. Therefore, this study aimed to investigate the potential toxicological mechanisms of palladium nanoparticles assessing their effects on normal diploid rat fibroblast and lung carcinoma human epithelial cell lines. Several endpoints such as cell growth, cell cycle progression, DNA damage, induction of apoptosis, reactive oxygen species production and expression of cell cycle regulatory proteins were evaluated. Results showed that palladium nanoparticles inhibited cell growth in a dose- and time-dependent manner in both cell lines, although with a more evident action on fibroblasts. Interestingly, inhibition of cell growth was not associated with the induction of apoptosis. Cell cycle progression was arrested in the G0/G1 phase and DNA damage was evident in both cell lines even if only a slight increase in the intracellular reactive oxygen species levels was detected. These findings provide valuable insight into understanding the molecular mechanisms responsible of palladium nanoparticles toxicity whose identification is essential to define an adequate risk assessment process.